Is CFIDS/ME a mitochondrial disease? Yes and no.
Mitochondrial diseases are mainly thought to affect the
mitochondria and science has long postulated that this
is the case with CFIDS/ME. More recently, that become
a proven scientific fact (Hokama et al*) but what that
research team found was that the ciguatera epitope is
found in all autoimmune diseeases and that the epitope,
which is very much like ciguatera, targets the mitochondria
along with other areas of the body.

The mitochondria are like little energy factories in
every cell of the body. There are hundreds of mitochondria
in each cell, zillions in the body, and they take in
oxygen and glucose and they put out carbon dioxide and
adenosine triphosphate (APT). APT is the essential form
of stored energy of the body. Think of it as your own "energizer" battery.
ATP is 3 phosphates which are converted to ADP which
is 2 phosphates. In a helathy person, the ATP recylces
about every ten seconds but slower cycling is a hallmark
of CFIDS/ME. The oxidative phosphorylationn (oc-phos)
are a very complex transportation chain of electrons
that do the major work. This is an essential part for
every organ system in the body.

But mitochondrial diseases are thought of by most medical
practitioners as diseases that are quickly fatal and
that strike the very young. While CFIDS/ME certainly
strikes the young (the youngest diagnosed patient in
the US was just two), it is not quickly fatal. Yet the
symptoms of mitochondrial diseases include neurological
symptoms including ataxia which is a loss of coordination,
myoclonis which is involuntary jerking of the muscle,
encephalitis which is a disease of the brain, exercise
intolerance, constipation and a sensitivity to anesthesia.
That is a description of CFIDS/ME! In fact, the sensitivity
to anesthesia has been proven to be when the same pathway
to the body is used for anesthesia that the ciguatera
epitope uses. The National CFIDS Foundation, in fact,
funded research to find the exact part of the sodium
channel** being used that must be avoided by all CFID/ME
patients and, it seems more than apparent, all those
with mitochondrial diseases that are, in fact, autoimmune
diseases.

When medical practitioners, however, diagnose a mitochondrial
disease, they usually require muscle biopsies and ox-phos
testing yet oxphos are usually found to be normal in
CFIDS/ME! Most physicians think of diseases as organ
specific and the mitochondria affect every organ in the
body. The main problem patients have for their reason
for disability is that they cannot sustain any level
of activity. That is because the recyling process is
far too slow with CFIDS/ME and the patient who tries
to push themselves find themselves in what they term
a "crash". The problem with the mitochondria
has been found by many researchers. Even Dr. Walter Tarello
found it in animals who had CFIDS/ME***. Yet Plioplys
and Ploiplys tested the mitochondria with electron microscopy
and found no differences in the structure although they
admitted the dysfunction could be functional. Years before
their own paper was published, it had been scientifically
proven that part of CFIDS/ME was apoptosis (cell death).
The mitochondria, it should be noted, play an important
role in the regulation of cell death.

An insufficient supply of ATP molecules means the patient
has insufficient energy which is called "chronic
fatigue". "Chronic fatigue" is a symptom
of insufficient molecular energy and, of course, our
Centers for Disease Control and Prevention (CDC), in
it's infinite wisdom, called this state of accelerated
oxidative molecular injury "chronic fatigue syndrome".

Dr. Alan Krensky, a deputy director of the National
Institutes of Health where mitochondrial research is
one of the six priority areas of new funding over the
next five years, said, "All these diseases --- diabetes,
cancer, atherosclerosis --- the major diseases of mankind,
appear to have major mitochondrial components." In
2003, researchers found genes involved in the mitochondira
were less active, for instance, in Type 2 diabetes. Other
researchers, who bred rats with little capacity for aerobic
exercise, found evidence of impaired mitochondria function
while other studies linked cancer, Parkinson's and Alzheimer's
to the mitochondria. One pharmacuetical giant, GlaxoSmithKline,
through Sirtris Pharmaceuticals, is working on drugs
that can increase the number of mitochondria as well
as boosting their function including one based on resveratrol.

The main problem of calling CFIDS/ME a mitochondrial
disease is that science has yet to catch up. Last fall,
researchers at the Roswell Park Cancer Institute (Cancer
Biol and Ther, Singh, Smiraglia) found dysfunction of
the mitochondria were alterations that are linked to
cancer. Mitochondria contain their own DNA and changes
are associated with the development of cancer. Didn't
the National CFIDS Foundation (NCF) point that out already?
Do you remember the headline of the first article in
the last edition about the NCF already funding a study
on leukemia? Our medical committee is thankful that the
NCF is not waiting for science to play catch-up! We need
more answers today and their research direction is not
just pointing the way but leapfrogging the staid and
slow movement of most research endeavors.